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Biomedical subjects

N Yuki

Publications and source records attributed to N Yuki.

At least 253 records · Page 14Linked to original sources
PubMed1993

Human leukocyte antigens in Fisher's syndrome.

We performed human leukocyte antigens (HLA) typing for class I antigens on 19 Japanese patients with Fisher's syndrome. We demonstrated a statistically significant association between the disease and the HLA-B39 antigen.

Disease Susceptibility↗
PubMed1993

Low prevalence of hepatitis C virus antibodies in chronic liver disease in northwest China.

To evaluate the prevalence of hepatitis C virus infection in northwest China, 179 chronic liver disease patients in this area were examined for antibody to hepatitis C virus core protein (anti-HCVcore). This antibody was found in only 5 (14 percent) of 37 chronic non-A, non-B liver disease patients, in 11 (16%) of 67 asymptomatic hepatitis B virus carriers, and in 20 (27%) of 75 chronic hepatitis B patients. High titers of anti-HCVcore (cut off index > 2) were observed in 3 (60%), 5 (45%), and 9 (45%) of the anti-HCVcore-positive cases of these groups, respectively. We further investigated the seroprevalence of antibodies to hepatitis B virus in the 37 chronic non-A, non-B liver disease patients. All 5 anti-HCVcore-positive cases were positive for a hepatitis B virus marker, with only 44% (14/32) of the anti-HCVcore-negative patients (P < 0.05). Based on these findings, it is concluded that the prevalence of hepatitis C virus infection in chronic non-A, non-B liver disease is unexpectedly low in northwest China and that hepatitis B and C viruses seem to have a similar mode of infection in that area.

Adult↗
PubMed1993

Prevalence of hepatitis C virus in family members of patients with hepatitis C.

To investigate the prevalence of hepatitis C virus in the family members of patients with hepatitis C, we examined antibody to hepatitis C virus with a second-generation enzyme-linked immunosorbent assay and viral RNA with a combined assay of reverse transcription and polymerase chain reaction in sera. Among 219 (75 spouses, 110 children, and 34 others), 26 (12%) were antibody positive. The positive rate of antibody to hepatitis C virus was significantly higher than that of the control group (2.0%) and of volunteer blood donors in our district (1.5%), and it increased with age. In particular, the positive rate of antibody to hepatitis C virus among spouses was high (24%). Among family members with elevated ALT, 59% were antibody positive, which was significantly higher than that of the control group (11%). Of the 26 who were antibody positive, 21 (81%) had viral RNA, whereas of the 70 who were antibody negative, only one (1.4%) had viral RNA. These data suggest that hepatitis C virus was transmitted by the infrafamilial route during long duration of contact with patients or sexual transmission. In family members, hepatitis C viral infection is the main cause of liver disorder, and many who were antibody-positive with a second-generation enzyme-linked immunosorbent assay had viremia in the sera.

Adolescent↗
PubMed1993

Association of IgG anti-GD1a antibody with severe Guillain-Barré syndrome.

We earlier reported cases of 2 patients with severe acute Guillain-Barré syndrome (GBS) associated with high-IgG anti-GD1a antibody titer. We now have investigated the autoantibody against GD1a or GM1 in 37 GBS patients using the enzyme-linked immunosorbent assay and have found a statistically significant association between IgG anti-GD1a antibody and the severity of the disease (need of a respirator for more than 1 month and a poor functional prognosis 3 months after neurologic onset). An autopsy which showed severe GBS associated with IgG anti-GD1a antibody produced the following findings: (1) severe axonal degeneration and segmental demyelination of peripheral nerves; (2) lymphocytic infiltration; and (3) marked central chromatolysis of the lower motoneurons.

Adolescent↗
PubMed1993

Antibodies to hepatitis C virus and hepatitis C virus infection.

The authors studied the interrelationship of antibody to hepatitis C virus core protein (anti-HCV core), antibody to C100-3 antigen (anti-C100-3) and serum hepatitis C virus RNA positivity in chronic liver disease patients. Anti-HCVcore was detected with high titers in 95% (69/73) of chronic non-A, non-B hepatitis patients, while anti-C100-3 was found in 60% (44/73). A close relationship was observed between detection of anti-HCVcore and viremia. Anti-HCVcore was also detected with low titers in 24% (10/41) of hepatitis B virus carriers negative for anti-C100-3. Hepatitis C virus RNA was found in 3 of the 10 anti-HCVcore-positive carriers. A significant correlation was observed between the occurrence of high titers of anti-HCVcore and serum hepatitis C virus RNA positivity. In chronic hepatitis C patients treated with interferon-alpha, a sustained reduction of anti-HCVcore was more closely associated with sustained virus clearance than that of anti-C100-3. These results indicate that anti-HCVcore may serve as a reliable marker of hepatitis C virus infection.

Antigens, Viral↗
PubMed1993

An immunologic abnormality common to Bickerstaff's brain stem encephalitis and Fisher's syndrome.

The nosological position of Bickerstaff's brain stem encephalitis (BBE) has yet to be established, and its etiology is not clear. Because anti-GQ1b antibody frequently occurs in patients with Fisher's syndrome (FS) and there are clinical similarities between FS and BBE, we investigated anti-ganglioside antibodies in sera from 3 BBE patients who had transient long tract signs in addition to acute ophthalmoplegia and cerebellar-like ataxia in order to clarify the etiology and nosological position of BBE. High IgG anti-GQ1b antibody titers were present in all 3 sera samples but decreased with the clinical course of the illness. In contrast, no anti-GQ1b antibody was found in sera from patients with other neurologic diseases which were able to produce transient brain stem disturbance: multiple sclerosis, neuro-Behçet's disease, brain stem infarction, herpes simplex virus encephalitis, and Wernicke's encephalopathy. The finding that BBE and FS shared common autoantibody suggests that autoimmune mechanism common to FS is likely in BBE, and that both conditions represent a distinct disease with a wide spectrum of symptoms that include ophthalmoplegia and ataxia.

Adult↗
PubMed1993

Serodiagnosis of chronic hepatitis C in Japan by second-generation recombinant immunoblot assay.

The seroprevalence of antibodies to hepatitis C virus (HCV) by a second-generation recombinant immunoblot assay (RIBA-2) was tested using 4 recombinant antigens. The results were correlated with those of C100-3 enzyme-linked immunosorbent assay (ELISA) and with the detection of HCV-RNA sequences by the polymerase chain reaction. Sera were obtained from 27 C100-3 ELISA-positive Japanese patients with chronic non-A, non-B liver disease and from 29 C100-3 ELISA-negative patients. All C100-3 ELISA-positive patients and 19 (66%) out of 29 C100-3 ELISA-negative patients reacted to two or more RIBA-2 antigens (reactive by RIBA-2). Of the remaining 10 C100-3 ELISA-negative patients, one patient reacted to just one antigen (indeterminate by RIBA-2), while 9 reacted to none of the 4 antigens (non-reactive by RIBA-2). Forty-three (93%) of the 46 RIBA-2-reactive patients and the single RIBA-2-indeterminate patient tested positive for HCV-RNA sequences, whereas only one (11%) of the 9 RIBA-2-non-reactive patients tested positive. These findings indicate that HCV infection is more prevalent than expected from the results of C100-3 ELISA, and that RIBA-2 is a more sensitive assay for estimating the presence of HCV infection in chronic liver disease.

Aged↗
PubMed1993

Frequent presence of anti-GQ1b antibody in Fisher's syndrome.

We used the enzyme-linked immunosorbent assay to investigate autoantibodies against the gangliosides GM1, GD1a, GD1b, GT1b, GD2, and GQ1b in sera from 16 patients with Fisher's syndrome. We found high anti-GQ1b antibody titers, mainly those of the IgG class, in the sera of 13 of these patients. The titers decreased with the clinical course of the illness. Moreover, anti-GQ1b antibody-positive patients had more severe ataxia of cerebellar type than the antibody-negative patients.

Adult↗
PubMed1993

[Serodiagnosis of hepatitis C by a recombinant hepatitis C virus protein].

Anti-HCV prevalence was high in chronic non-A, non-B liver disease. Anti-C100-3 was detected frequently in each category of chronic non-A, non-B liver disease. Antibody to HCV core protein was detected more frequently in 95% with high titers. A significant correlation was observed between the occurrence of high titers of antibody to HCV core and serum HCV RNA positivity. In patients negative by the anti-C100-3 assay, 69% were anti-HCV-positive by the second-generation enzyme-linked immunosorbent assay and also positive by the reverse transcription-polymerase chain reaction. Thus, HCV is a major causative agent of chronic non-A, non-B hepatitis in Japan.

Antigens, Viral↗
PubMed1993

Changes in antibodies to specific hepatitis C virus antigens with interferon-alpha therapy: analysis by recombinant immunoblot assay.

Antibodies to hepatitis C virus NS3 (C33C), NS4 (5-1-1 and C100-3), and core (C22-3) proteins were tested for by a second-generation recombinant immunoblot assay of serum samples from 42 chronic hepatitis C patients treated with interferon-alpha. Antibodies to 5-1-1 and C100-3 were found in 83% (35/42) before therapy, and those to C22-3 and C33C in all patients. At 6 months after therapy withdrawal in patients with sustained virus clearance, only antibodies to 5-1-1 and C100-3 showed significant decreases (p < 0.05) (5/5 and 7/7, respectively). Antibodies to C22-3 and C33C decreased less frequently in only 11% (1/9) (p < 0.01) and 44% (4/9) (p < 0.05), respectively. Thus, antibodies to 5-1-1 and C100-3 are prone to decrease following a decline in viremia. The antibody to the C22-3 (core) protein was least likely to decrease and may serve as a reliable marker of exposure to the virus.

Adult↗
PubMed1993

Quantitative analysis of antibodies to hepatitis C virus during interferon-alpha therapy.

We quantified IgG antibodies to structural (core) and nonstructural (C100-3) hepatitis C virus proteins in 42 patients with chronic hepatitis C treated with a 6-mo course of interferon-alpha. Sera were drawn before and at the end of therapy and also 6 mo after therapy withdrawal; they were stored for later analysis of antibodies and serum hepatitis C virus RNA. Sustained virus clearance was observed at the end of therapy and 6 mo after therapy withdrawal in nine cases; it was accompanied with sustained reductions of antibody to hepatitis C virus core protein and antibody to C100-3 protein. A sustained reduction of antibody to hepatitis C virus core protein was specific to sustained virus clearance, although that of antibody to C100-3 protein was not. None of the patients who did not show reductions of levels of both antibodies at the end of therapy displayed sustained virus clearance. Five patients showed hepatitis C virus RNA negativity and normal aminotransferase levels at the end of therapy without reduction of antibody to hepatitis C virus core protein levels. Of these five patients, relapse of hepatitis occurred in four, and viremia was present 6 mo after therapy withdrawal in all cases. These results demonstrate that testing for antibody titers may add information for evaluating virus clearance after interferon therapy.

Adult↗
PubMed1993

[Proximal lower motor neuron syndrome associated with serum antibodies to asialo-GM1, GM1 and LM1].

A 31-year-old man had noticed slowly progressive weakness in his right upper limb girdle. On admission at age 32, fasciculation and muscle atrophy were observed in the right pectoralis major muscle. There was mild muscle weakness in the right triceps brachii muscle. The deep tendon reflexes were normal and the pathologic reflexes were absent. Sensory and autonomic nerve functions were intact. Needle EMG showed fibrillation potentials and positive sharp waves in the right pectoralis major, infraspinatus, extensor carpi radialis, extensor digitorum muscles, the bilateral sternocleidomastoideus and triceps brachii muscles. Motor nerve conduction studies revealed normal conduction velocities and distal latencies as well as no evidence of conduction block or abnormal temporal dispersion. Serum immunoelectrophoresis failed to detect an M protein. Thin-layer chromatography with immunostaining revealed that the serum contained auto antibodies which reacted with asialo-GM1, GM1 and LM1. This case must belong to "proximal lower motor neuron syndrome" proposed by Pestronk et al.

Adult↗
PubMed1993

[An acute axonal form of Guillain-Barré syndrome with autoantibody against ganglioside GD1b--a case report].

We reported a 3-year-old boy of an acute axonal form of Guillain-Barré syndrome (GBS) with autoantibody against GD1b ganglioside. A week after an episode of upper respiratory infection, he was hospitalized with a weakness in the lower extremities. Neurological examination revealed facial weakness, restricted extra-ocular movement, hyporeflexia and tetraparesis without any sensory impairment. CSF protein was elevated with normal cell count after the first week of symptoms. Electrophysiological studies demonstrated normal motor nerve conduction velocity and low M potential amplitude. He had been on a respirator for two months. Although he received plasmapheresis in the acute phase, sixteen month after the onset he continued to have distally dominant limb weakness with wasting. Thin-layer chromatogram with immunostaining revealed that serum IgG from this patient reacted with GD1b, but did not react with GM1. Enzyme-linked immunosorbent assay showed that anti-GD1b titer (IgG) decreased concurrently with the clinical improvement. There have been several reports of an acute axonal form of GBS with antibody to GM1. GD1b, as well as GM1, seems to be a target pathogenic antigen in motor axon disorders.

Autoantibodies↗